Modern methods of diagnosis and treatment of chronic renal failure. Impaired glomerular filtration of the kidneys Classification of chronic kidney disease

A decrease in kidney function until the complete cessation of their filtration capabilities and the ability to remove toxins from the body is chronic renal failure. The etiology of this disease is a consequence of previous diseases or the presence of chronic processes in the body. This kidney damage is especially often diagnosed in older people. Chronic renal failure is a fairly common kidney disease and the number of patients is growing every year.

Pathogenesis and causes of chronic renal failure

• chronic kidney disease - pyelo- or glomerulonephritis;
• systemic disorders metabolic processes- vasculitis, gout, rheumatoid arthritis;
• the presence of cameos or other factors (mucus, pus, blood) blocking the ureter;
• malignant neoplasms of the kidneys;
• neoplasms of the pelvic organs, in which compression of the ureter occurs;
• disorders in the development of the urinary system;
• endocrine diseases (diabetes mellitus);
• vascular diseases (hypertension);
• complications of other diseases (shock, poisoning with toxic drugs);
• alcohol and drug use.

The pathogenesis of this disease is a consequence of the above reasons, in which chronic damage and structural disorders of the renal tissue develop. The process of parenchyma restoration is disrupted, which leads to a decrease in the level of functioning kidney cells. At the same time, the kidney decreases in size and wrinkles.

Symptoms and signs of the disease

Malaise, fatigue, loss of appetite, nausea and vomiting are symptoms of chronic renal failure.

Signs of chronic renal failure occur against the background of removing toxins, as well as maintaining metabolic processes, which leads to a malfunction of all systems and organs of the body. Symptoms of chronic renal failure are mild at first, but as the disease progresses, patients experience malaise, fatigue, dry mucous membranes, changes in laboratory tests, insomnia, nervous twitching of the limbs, tremor, numbness of the fingertips. As the disease progresses, the symptoms worsen. Persistent (morning and around the eyes), dry skin, loss of appetite, nausea, and hypertension develop. Forms of chronic renal failure are divided into five stages depending on the severity of the course.

Classification by stages

• Stage 1 CKD is latent. Passes without significant symptoms. Patients do not complain of anything except increased fatigue. In laboratory tests there is a small amount of protein.
• CKD stage 2 - compensated. Patients have the same complaints, but they appear more often. There are changes in laboratory parameters in urine and blood. There is an increase in the daily amount of urine excretion (2.5 l).
• CKD stage 3 - intermittent. There is a further decrease in kidney function. In blood tests increased level creatinine and urea. There is a deterioration in the condition.
• CKD stage 4 - decompensated. A severe and irreversible change occurs in the functioning of this internal organ.
• CKD stage 5 - end-stage chronic renal failure is characterized by the fact that kidney function almost completely stops. There is a high content of urea and creatinine in the blood. Changes electrolyte metabolism in the kidneys, uremia occurs.

The stages of chronic renal failure are classified depending on the degree of damage to the parenchyma of the organ, its excretory functions and have five degrees. The stages of chronic kidney disease are distinguished according to two criteria - glomerular filtration rate, creatinine and protein level in the urine.

Classification of chronic kidney disease by GFR

Indexation of CKD by albuminuria level

Kidney damage in children

Chronic kidney disease is rare in children, but it is at this age that these disorders are very dangerous.

Chronic kidney disease in children is uncommon, but isolated cases do occur. This is a very dangerous disease because it is in childhood With such violations, kidney failure occurs, which leads to death. Therefore, identifying chronic renal failure and CKD at the earliest stages is an important task in pediatric nephrology. The causes of CKD in children are:

• low birth weight;
• prematurity;
• abnormalities of intrauterine development;
• renal vein thrombosis in newborns;
• past infectious diseases;
• heredity.

The classification of chronic disease in adults and CKD in children is the same. But the main sign that a child has this disease is that it occurs in school-age children. The main manifestation of the syndrome is a sharp disruption of the kidneys and, as a result, severe intoxication of the body. Urgent hospitalization is required.

Complications of the disease

This is a very dangerous disease, the 1st stage of which occurs with hidden symptoms, and the 2nd stage with mild signs of the disease. Chronic renal failure should be treated as early as possible. Chronic renal failure in the initial stage is not characterized by profound changes in the renal tissue. With CKD stage 5, irreversible processes develop that lead to poisoning of the body and deterioration of the patient’s condition. Patients experience arrhythmia, albuminuria, persistent hypertension, anemia, confusion up to coma, nephrogenic hypertension, angiopathy, heart failure and pulmonary edema may develop. Exacerbation of CKD and chronic renal failure leads to uremia. In this case, urine entering the blood leads to uremic shock, which often leads to death.

Diagnosis of the disease

Diagnosis of CKD involves consulting doctors:

• therapist;
• urologist;
• cardiologist;
• endocrinologist;
• ophthalmologist;
• neurologist;
• nephrologist.

Diagnosis of CKD involves taking an anamnesis, after consultation with a number of specialists, and a fairly objective examination.

The doctor will collect an anamnesis (all symptoms of the disease, concomitant diseases, in children - the presence of physical developmental delay, as well as features of the family history). An objective examination includes percussion and palpation of the kidneys. In children - examination of the ridge, the presence of weight deficiency, stunted growth, the presence of high blood pressure, signs of anemia, etc. Chronic renal failure is determined by tests:

• Urinalysis - a small amount of protein, decreased density, the presence of red blood cells, casts and an increased number of leukocytes.
• A blood test reveals an increase in leukocytes and ESR, a decreased amount of hemoglobin and red blood cells.
• Biochemical analysis - increased creatinine, urea, nitrogen, potassium and cholesterol in the blood. Decreased protein and calcium.
• Determination of glomerular filtration rate - calculated based on a blood test for creatinine, age, race, gender and other factors.
• An ultrasound of the kidneys and urinary system will help to see the condition of the kidney.
• MRI visualizes the structure of the kidney, its components, ureter and bladder.
• Doppler ultrasound evaluates the condition of the kidney vessels.
• Zimnitsky test - shows the state of kidney function, and you can also see the volume of urine excreted in the morning and afternoon.

Treatment of kidney failure

Initially, treatment of chronic kidney disease is aimed at reducing blood pressure, improving urine formation, lowering the pH of the stomach, and normalizing microelements in the blood. Later, depending on the patient’s condition, hemodialysis, peritoneal dialysis or kidney transplantation are prescribed. With this disease, you should not overcool, lift heavy objects, or succumb to stressful situations. It is very important to adhere to proper nutrition. Patients are prescribed diet No. 7. Its main principles are: limited protein intake, reducing the amount of salt and phosphorus in food, reducing and monitoring the amount of potassium, controlling fluid intake (no more than 2 liters), controlling the energy value of food. Nutrition for CKD is not similar to the usual fasting during illness; the menu should include enough fruits and vegetables in the form of soups and compotes.

Limiting protein intake is already recommended at the beginning of the disease - up to 1 g/kg, then - 0.8 g/kg, and at other stages - 0.6 g/kg. Controlling salt intake is a very important point in the diet, since an excess of sodium in the blood leads to hypertension and edema, so it is recommended to consume no more than two grams per day. They also limit the intake of phosphorus to 1 g per day (limit the consumption of foods high in phosphorus). To reduce potassium in the body, which can lead to cardiac arrest, dried fruits, bananas, avocados, potatoes, greens, nuts, chocolate, and legumes are excluded from the diet. The energy value of food should be 2.5-3 thousand calories. The patients' diet is divided (5-6 times, in small portions). The menu should be rich in fruits and vegetables in the form of compotes, soups, etc. Take food boiled or baked.

The diet should include the following products:

• cereals;
• whole grain bread;
• dietary soups;
• meat and fish products from low-fat varieties;
• vegetables and fruits;
• eggs;
• milk, cottage cheese;
• jellies and mousses;
• diluted juice and weak tea, rosehip decoction;
• spices.

Contraindicated:

• salty and spicy foods;
• alcoholic drinks, strong teas, coffee.
• mushrooms;
• greenery;
• legumes and pasta;
• smoked and preserved;
• bananas and dried fruits;
• seasonings: mustard and horseradish;
• garlic and radish.

occurs due to kidney damage. Normal, healthy kidneys remove waste and excess water from the blood, which is excreted from the body in the form of urine. The kidneys are also involved in controlling blood pressure and producing red blood cells (RBCs). In chronic kidney disease, the kidneys' function is impaired, so they cannot remove waste from the blood as well as healthy kidneys.

Causes of chronic kidney disease

The most common causes of chronic kidney disease are high blood pressure, diabetes and heart disease. Chronic kidney disease can also be caused by infections, autoimmune kidney damage, and urinary obstruction.

Most people have no early symptoms of chronic kidney disease. As chronic kidney disease progresses, the following symptoms appear:

• fatigue, fatigue
• loss of appetite
• insomnia
• swelling of the legs and ankles
• memory impairment, absent-mindedness.

Diagnosis of chronic kidney disease

There are three simple tests that will allow the doctor to suspect chronic kidney disease:

• blood pressure measurement
• determination of protein in urine
• determination of creatinine in blood serum.

How to slow down the progression of chronic kidney disease?

If you suffer from hypertension, it is important to control your blood pressure. Angiotensin-converting enzyme blocker medications and angiotensin II blocker medications reduce high blood pressure and also have a nephroprotective effect, that is, they prevent the worsening of chronic kidney disease.

Moderate exercise and a healthy diet also help lower blood pressure.

If you suffer from diabetes, your doctor will give you recommendations on how to maintain normal blood sugar levels.

If you smoke, then quit smoking. Smoking damages the kidneys. Smoking also increases blood pressure and interferes with the effectiveness of medications that lower blood pressure. Your doctor will prescribe you a low protein diet. The high protein content in food makes it difficult for the affected kidneys to work.

You should have regular checkups with your doctor. This way, the doctor can monitor kidney function and treat problems associated with chronic kidney disease.

Chronic kidney disease can cause other problems:

• High cholesterol
• Anemia. Anemia occurs when there is insufficient level of hemoglobin in the blood (a protein that transports oxygen from the lungs to other organs and tissues of the body). Symptoms of anemia include: fatigue, weakness.
• Bone damage. As a result of chronic kidney disease, the normal metabolism of minerals - phosphorus and calcium, which are necessary for strengthening bones - is disrupted. Your doctor will prescribe you a diet that limits certain foods so that your body can better absorb these minerals.

Chronic kidney disease causes loss of appetite. A nutritionist will help you plan a special diet.

What happens as chronic kidney disease progresses?

Even with proper treatment Chronic kidney disease gradually leads to impaired kidney function and progression of renal failure. At some point the kidneys stop working. Toxins accumulate in the body, which act as poison. Poisoning causes vomiting, weakness, impaired consciousness and coma.

Treatment for end-stage chronic kidney disease requires dialysis or kidney transplantation. During dialysis, a special machine called an artificial kidney is used to remove waste from the blood. There are two types of dialysis: hemodialysis and peritoneal dialysis. Hemodialysis is performed in a hospital setting. After training, the patient can perform peritoneal dialysis independently at home.

If you need dialysis, your doctor will determine the type of dialysis you need.

The term chronic kidney disease means that the kidneys have become abnormal. There are many diseases that lead to the development of chronic kidney disease. People suffering from chronic kidney disease of any stage are at risk for developing the disease of cardio-vascular system and stroke. Because of this, it is important to detect even mild chronic kidney disease, since treatment not only slows the progression of chronic kidney disease, but also reduces the risk of heart disease and stroke.

How do the kidneys work?

Kidneys- These are bean-shaped organs located in the lumbar region on either side of the spine.

The renal artery supplies blood to each kidney. In the kidney, the artery divides into many small blood vessels (capillaries), forming structures called the glomerulus.

Each glomerulus is a filter. The structure of the renal glomeruli allows waste, excess water and salt to pass from the blood into thin tubules. The liquid that remains at the end of each tubule is called urine. The urine then enters the renal collecting system, which is represented by the renal calyces and renal pelvis. The urine then travels through the ureter into the bladder. Urine is stored in the bladder and then removed from the body through the urethra (urethra).

The main functions of the kidneys are:

• Removal of waste, excess water from the blood, formation of urine
• Blood Pressure Control – The kidneys control blood pressure in part by removing excess water from the body through urine, and the kidneys also produce hormones that regulate blood pressure.
• The kidneys produce a hormone called erythropoietin, which stimulates the bone marrow to produce red blood cells (erythrocytes). Erythropoietin prevents the development of anemia.
• The kidneys maintain a certain level of salts and trace elements in the blood.

Chronic illness is a long-term, ongoing illness. Chronic illness does not always mean serious illness. Mild chronic kidney disease affects many people.

Chronic renal failure is a term synonymous with chronic kidney disease.

The term acute kidney failure means that kidney function declines suddenly over a period of hours or days. For example, the cause of acute renal failure may be a serious infection that affects the kidneys, or poisoning, such as alcohol substitutes. This distinguishes acute kidney failure from chronic kidney disease, in which kidney function declines gradually over months or years.

How is chronic kidney disease diagnosed?

A simple blood test can estimate the amount of blood that is filtered by the glomeruli over a given period of time. This test is called glomerular filtration rate determination. The normal glomerular filtration rate is 90 ml/min or more. If filtration does not occur or slows down in some glomeruli, the glomerular filtration rate (GFR) decreases, which allows us to conclude that renal function is impaired.

To determine the glomerular filtration rate in the blood, the level of creatinine is determined. Creatinine is a breakdown product of proteins. Normally, creatinine is removed from the blood by the kidneys. If kidney function is impaired, the level of creatinine in the blood increases.

Glomerular filtration rate is calculated taking into account age, gender and blood creatinine level.

Chronic kidney disease, depending on the level of glomerular filtration rate, is divided into five stages:

• Stage 1 - Glomerular filtration rate (90 ml/min or more) shows normal kidney function, but you have kidney damage or disease. For example, blood or protein may appear in the urine, or inflammation of the kidneys.
• Stage 2 – moderate impairment of kidney function and there is kidney damage or kidney disease. People whose glomerular filtration rate is 60 – 89 ml/min without kidney damage do not suffer from chronic kidney disease.
• Stage 3 – moderate renal dysfunction (without or with kidney disease). For example, in older people, kidney function decreases without any kidney disease: 3A glomerular filtration rate is - 45 - 59 ml/min; 3B glomerular filtration rate is 30 – 44 ml/min.
• Stage 4 – severe renal impairment. The glomerular filtration rate ranges from 15 to 29 ml/min.
• Stage 5 – extremely severe renal dysfunction. This condition is also called end-stage renal failure or kidney failure. Glomerular filtration rate less than 15 ml/min.

Note: Slight changes in glomerular filtration rate are normal. In some cases, fluctuations in glomerular filtration rate may be large enough to change the stage of chronic kidney disease, but after some time the glomerular filtration rate may increase again. However, as long as the glomerular filtration rate does not decrease progressively, the average value must be taken into account.

Who needs to measure glomerular filtration rate?

Glomerular filtration rate is usually tested to monitor kidney function in people with kidney disease or other conditions that can affect the kidneys, such as high blood pressure or diabetes. Glomerular filtration rate testing is also often performed during examinations in various medical situations. If the patient suffers from chronic kidney disease, the glomerular filtration rate is examined at regular intervals to monitor kidney function.

What is the incidence of chronic kidney disease?

About one in 10 people have some degree of chronic kidney disease. Chronic kidney disease can develop at any age. Various medical conditions can lead to chronic kidney disease. The incidence of chronic kidney disease increases in older people. Women are more likely to suffer from chronic kidney disease.

Although more than half of people over 75 years of age have chronic kidney disease, most of them do not actually have kidney disease, but age-related decline in kidney function.

Most cases of chronic kidney disease are moderate or moderate in severity.

What causes chronic kidney disease?

There are many medical conditions that can cause kidney damage and/or impairment of kidney function and lead to chronic kidney disease. The three main causes of chronic kidney disease, which occur in approximately 3 out of 4 cases of chronic kidney disease in adults, are:

• Diabetes mellitus – diabetic kidney damage (a common complication of diabetes mellitus)
• High blood pressure – Untreated or poorly controlled high blood pressure is a leading cause of chronic kidney disease. However, in some cases, chronic kidney disease itself is the cause of high blood pressure, since the kidneys are involved in its regulation. Nine out of 10 people with stage 3 to 5 chronic kidney disease have high blood pressure.
• Aging of the kidneys – there is an age-related decline in kidney function. More than half of people over 75 have some degree of chronic kidney disease. In most cases, chronic kidney disease does not progress beyond a mild stage unless the kidneys are affected due to other causes, such as diabetes.

Other conditions that may lead to the development of chronic kidney disease include:

• Glomerulonephritis (damage to the glomeruli)
• Renal artery stenosis
• Hemolytic uremic syndrome
• Polycystic kidney disease
• Blockage of urine flow
• Kidney damage due to poisoning from drugs or toxic substances
• Chronic kidney infections and others.

If you have moderate chronic kidney disease (that is, stages 1 to 3), you are unlikely to feel unwell. Chronic kidney disease is detected by testing the glomerular filtration rate before other signs and symptoms appear.

Symptoms develop as chronic kidney disease progresses. Symptoms are vague at first, characteristic of many diseases, such as increased fatigue, poor health, fatigue.

As the severity of chronic kidney disease increases, the following symptoms develop:

• malfunction
• loss of appetite
• weight loss
• dry skin, itching
• muscle spasms
• fluid retention in the body and the development of swelling of the legs
• puffiness around the eyes
• more frequent urination
• pale skin due to anemia
• weakness, fatigue.

If kidney function continues to deteriorate (stage 4 or 5 chronic kidney disease), various complications develop. For example, anemia and impaired phosphorus-calcium metabolism, increased levels of minerals in the blood. They can cause a variety of symptoms, such as fatigue due to anemia or thinning of bones and fractures due to calcium and phosphorus imbalances. Without treatment, stage 5 chronic kidney disease is fatal.

Do I need further examination?

Glomerular filtration rate is determined in order to identify chronic kidney disease and monitor its development. Glomerular filtration rate is measured at least once a year in patients with stage 1 or 2 chronic kidney disease, or more frequently in stage 3, 4, or 5 chronic kidney disease.

You will have routine urine tests to monitor for blood or protein in your urine. Blood tests will also be performed periodically to monitor levels of electrolytes in the blood, such as sodium, potassium, calcium and phosphorus. Your doctor will determine whether you need other tests. For example:

A kidney ultrasound (renal ultrasound) or kidney biopsy is prescribed if kidney disease is suspected. For example, if a large amount of blood or protein is detected in the urine, if you are worried about pain associated with the kidneys, and so on.

In most cases, a kidney ultrasound or kidney biopsy is not required. This is because chronic kidney disease typically occurs due to existing causes of kidney damage, such as complications of diabetes, high blood pressure, or age-related changes.

If chronic kidney disease progresses (stage 3 or more), additional studies are performed. For example, to detect anemia, a blood test is performed to determine the level of parathyroid hormone in the blood. The parathyroid hormone is involved in calcium-phosphorus metabolism.

How is chronic kidney disease treated?

In most cases, chronic kidney disease is treated by doctors general practice. This is due to the fact that stage 1–3 chronic kidney disease does not require treatment from a specialist. Your doctor will refer you to a specialist if chronic kidney disease progresses to stage 4 or 5, or if any stage of chronic kidney disease develops symptoms that require evaluation by a specialist.

Research has shown that for most patients with chronic kidney disease, treating the early stages of the disease can prevent or slow the progression of kidney failure.

Goals of therapy include:

• Treatment of the underlying disease
• Preventing or slowing the progression of chronic kidney disease
• Reducing the risk of development cardiovascular diseases
• Treatment of symptoms and complications caused by chronic kidney disease.

Treatment of the underlying disease

The development of chronic kidney disease can be caused by various diseases. For some of them there are specific treatment methods. For example, good blood sugar control for people with diabetes, blood pressure control for patients with hypertension, antibiotic treatment for patients suffering from chronic kidney infections, surgery to remove an obstruction to the flow of urine, and others.

Preventing or slowing the progression of chronic kidney disease:

Chronic kidney disease tends to gradually worsen over months or years. This can happen even if the underlying cause of chronic kidney disease is eliminated. You should be monitored by your doctor or nurse to monitor your kidney function (glomerular filtration rate). The doctor will also prescribe treatment for you and give recommendations on how to prevent or slow down the development of chronic kidney disease. The main goal of treatment to slow the progression of chronic kidney disease is to maintain optimal blood pressure. Most people with chronic kidney disease need medications to control their blood pressure. The doctor will determine the optimal blood pressure level for you (usually 130/80 mmHg or in some cases even lower).

If you are taking other medications, you should discuss your dosage regimen with your doctor. Since some medications, affecting the functioning of the kidneys, reduce their function, which worsens the course of chronic kidney disease. For example, if you suffer from chronic kidney disease, you should not take anti-inflammatory drugs without a doctor's prescription. You may also need to adjust the doses of medications you take if your chronic kidney disease progresses.

Reducing the risk of developing cardiovascular diseases:

People suffering from chronic kidney disease are in the group high risk on the development of cardiovascular diseases such as heart attack, stroke, peripheral vascular disease. People with chronic kidney disease are more likely to die from cardiovascular disease than from kidney failure.

Prevention of cardiovascular diseases includes:

• blood pressure control (and good blood sugar control if you have diabetes)
• blood cholesterol control
• Lifestyle changes: quitting smoking, eating a healthy diet low in salt, controlling weight, regular exercise.

If your urine test shows high levels of protein, you need treatment, even if your blood pressure is normal. Medicines called angiotensin converting enzyme blockers (eg captopril, enalopril, ramipril, lisinopril) for chronic kidney disease prevent further decline in kidney function.

Treating symptoms caused by chronic kidney disease

If chronic kidney disease progresses to severe form, then you need treatment to combat problems caused by poor kidney function. For example:

If anemia develops, treatment with iron supplements and/or erythropoietin is necessary. Erythropoietin is a hormone produced in the kidneys that stimulates the production of red blood cells (erythrocytes).

An imbalance of phosphorus and calcium in the blood also requires treatment.

You need to limit the amount of liquid and salt in your food. Other dietary restrictions involve controlling the level of potassium and calcium in the body.

If you develop end-stage chronic kidney disease, you need renal replacement therapy - dialysis or kidney transplantation.

People with stage 3 or more advanced chronic kidney disease should receive an annual flu shot and one pneumococcal vaccine. People with stage 4 chronic kidney disease should be vaccinated against hepatitis B.

Prognosis of chronic kidney disease

Chronic kidney disease stages 1 - 3 in most cases occur in older people. Chronic kidney disease tends to gradually get worse over months or years. However, the rate of progression varies from case to case and often depends on the severity of the underlying cause. For example, some kidney diseases can worsen kidney function relatively quickly. However, in most cases, chronic kidney disease progresses very slowly. At stage 5 of chronic kidney disease (glomerular filtration rate less than 15 ml/min), dialysis or a kidney transplant is required.

The article is for informational purposes only. For any health problems, do not self-diagnose and consult a doctor!

V.A. Shaderkina - urologist, oncologist, scientific editor

Pathogenetic therapy of renal acidosis should include not only eliminating the deficiency of buffer bases, but also improving the acid-excreting function of the kidneys. The main cause of acidosis in a number of patients is the retention of hydrogen ions, which, according to some authors, cannot be relieved by infusion of alkaline solutions. It is more correct, in their opinion, to use dialysis for this purpose, which helps remove excess hydrogen ions. However, this situation appears to be true only for very severe patients with oligoanuria. Our study of the acid-secreting function of the kidneys during repeated intravenous infusions of alkaline solutions showed that, as a result of acidosis correction, in some patients not only does the plasma concentration of bicarbonates increase, but also the release of hydrogen ions (mainly in the form of ammonium salts) by the kidneys increases significantly (Fig. 66).

Rice. 66. The effect of intravenous drip infusions of 1.3% sodium bicarbonate solution on the acid excretion function of the kidneys in patients with renal failure.

An increase in the acid-secreting capacity of the kidneys in this case may be associated with an increase in the filtration charge of sodium and an increase in ion exchange processes in the tubules (exchange of sodium for hydrogen ions and ammonia), with the development of intracellular acidosis due to the loss of intracellular potassium, as well as with an increase in filtration and diuresis. In general, it should be emphasized that the introduction of alkaline solutions when correcting acidosis has a very wide range of action, and its significance is by no means limited to replenishing the alkaline reserve of the blood. In patients in the phase of renal failure, but with preserved diuresis, during the correction of acidosis, sodium excretion significantly increases, the nitrogen and acid excretion function of the kidneys improves, it is often possible to stop the hyperkalemia and hyperphosphatemia accompanying acidosis, and also to achieve a certain clinical improvement. The following example is indicative in this regard.

Patient P., 38 years old. Diagnosis: chronic diffuse glomerulonephritis. Uremia, anemia. Delivered to the nephrology department on 9/VIII 1967 with signs of uremic coma. Pulse 84 beats per minute, satisfactory filling. The borders of the heart are expanded to the left, the sounds are dull. Blood pressure 190/110-220/120. Blood test: Hb - 38 units, er. - 2,400,000, l. - 17,500, ROE - 47 mm per hour. Residual nitrogen - 75-108 mg%, creatinine - 7.2-8.1 mg%. Daily diuresis is about 2 liters. The specific gravity of urine when tested according to Zimnitsky is 1003-1006. In the Kakovsky-Addis test there are 490 million red blood cells, 17 million leukocytes, 1 million casts. Urine analysis 10/VIII 1967: specific gravity - 1005, protein -2.6%, leukocytes - 15-30 in the field of view , fresh and leached red blood cells cover the entire field of view, cylinders are hyaline and granular 0-2 in the field of view. Glomerular filtration by endogenous creatinine - 11.4 ml/min, secretion of phenolrot dye - 5%. Blood electrolytes: sodium - 130.5-135 meq/l, potassium - 5.1-6.65 meq/l, calcium - 14.2 mg%, phosphorus - 8.1 mg%, chlorine - 88.1 meq/ l. Urinary excretion per day: sodium - 98-123 mEq, potassium - 54.5-87 mEq, chlorine - 40-96 mEq, bicarbonates - 9-23.6 mEq. Indicators of acid-base balance: blood pH - 7.26, base deficiency - 12 meq/l. Standard bicarbonate is 16 mEq/L. pCO 2 blood - 40 mmHg; Urine pH is 7.5-8.1. Urinary excretion: ammonia - 20-32 meq per day, titratable acids - 0. Total excretion of hydrogen ions - 20-32 meq per day.

Treatment: antihypertensive therapy, cardiac, anabolic hormones, intestinal and gastric lavage, subcutaneous and intravenous administration of saline and glucose, a diet with limited protein and sufficient salt. During two weeks of hospital stay, the patient's condition improved somewhat, however, despite sufficient diuresis, high azotemia and creatinemia, hyperphosphatemia, and hyperkalemia persisted. Due to severe acidosis, it was decided to resort to intravenous administration of alkaline solutions. For 10 days, a 1.3% sodium bicarbonate solution was administered intravenously daily or every other day at a dose of 10 ml per kg of body weight per day (Fig. 67). As a result of the administration of bicarbonate, it was possible to normalize the acid-base balance of the blood. Sodium excretion increased significantly, reaching 293.4 mEq per day. The excretion of organic acids increased (from 28.4 to 54.7 mEq per day) and phosphorus (from 3.6 to 5 g per day). At the same time, the excretion of chlorine and potassium increased relatively little, and the excretion of bicarbonate increased significantly only towards the end of the course of infusions. Thus, a significant part of sodium was excreted with anions of organic acids, sulfates and phosphates, which helped to reduce uremic intoxication. The excretion of hydrogen ions increased significantly (up to 80-100 meq per day) (mainly due to an increase in ammonia excretion). During the entire treatment period, the patient was administered 464 mEq of sodium in the form of bicarbonate; in addition, he received about 1020 mEq of sodium from food. During the same period, 1897 mEq was excreted in urine, about 20 mEq in feces, and the patient lost some sodium through sweat. Thus, despite the introduction of a significant amount of sodium bicarbonate, the sodium balance during the period of correction of acidosis was negative, i.e., loss of this ion was observed mainly in the urine. An increase in sodium excretion in urine leads to an increase in diuresis, which in this case is osmotic in nature. The relationship between urinary sodium excretion and increased urine output during acidosis correction is shown in Fig. 68 using the example of a patient with renal failure. Osmotic diuresis, apparently, is one of the mechanisms that helps reduce azotemia, hyperphosphatemia, hyperkalemia, as well as the elimination of excess acid radicals in patients receiving alkaline solutions. As can be seen from Fig. 67, as a result of intravenous administration of sodium bicarbonate solution to patient P., his diuresis almost doubled, reaching 3-4.5 liters per day. Glomerular filtration increased from 11.4 to 14.3 ml/min. Residual blood nitrogen decreased from 72 to 48 mg%, creatinine - from 7.2 to 4.2 mg%, inorganic phosphorus - from 8.1 to 4.3 mg%, potassium - from 6.65 to 4.7 mEq/ l. The administration of bicarbonate led to a slight decrease in plasma chlorine concentration (from 88.1 to 82.9 mEq/L). At the same time, plasma bicarbonate concentration increased from 16 to 23 mEq/L, and natremia reached the upper limit of normal (150 mEq/L). Thus, the observed loss of sodium appears to have been associated mainly with the removal of excess sodium from tissues, while its plasma level even increased slightly. Despite the latter circumstance, not only was there no increase in blood pressure, but, on the contrary, there was a tendency towards its normalization, which can partly be explained if we take into account that the value of blood pressure is affected not only by the level of natremia, but also by the sodium content in the vascular wall. As noted above, the acid-base balance in the blood returned to normal, and excess bicarbonate was excreted in the urine. The patient's general condition improved significantly.

Rice. 67. The effect of intravenous drip infusions of 1.3% sodium bicarbonate solution on the acid-base balance, residual nitrogen, creatinine, potassium and blood phosphorus in patient P., 38 years old, with chronic glomerulonephritis and renal failure.
SB - standard bicarbonate, meq/l; BE - base deficiency, mEq/L.

Rice. 68. The relationship between sodium excretion (1) and diuresis (2) with intravenous administration of 1.3% sodium bicarbonate solution to patients with renal failure.

It should be emphasized that the above-mentioned positive dynamics of acid-base balance indicators in the process of intravenous correction of acidosis is short-term in nature. More or less long-term normalization of acid-base balance can be achieved, as a rule, only as a result of daily infusions. When alkalizing solutions are administered every other day, the correction is usually worse, and more infrequent injections are often ineffective. However, even a relatively short-term course of alkalizing therapy (as can be seen in the example above) in some cases contributes to the onset of general clinical remission.

In patients with acute nephritis, alkali therapy is usually not indicated due to the risk of introducing large amounts of sodium and fluid, which can adversely affect the course of the disease, aggravate edema and hypertension. However, in acute nephritis, which occurs with severe acidosis and uremia, an attempt at such treatment, subject to constant monitoring of blood pressure levels and blood electrolytes, is justified.

Alkalinizing therapy is widely used in patients with chronic kidney disease, especially in the phase of renal failure, as well as in cases where acidosis is accompanied by a significant loss of bicarbonates. Intravenous drip infusions of isotonic, 1.3% sodium bicarbonate solution lead to quick and effective correction of acidosis. For moderate acidosis, 10-15 ml of solution per kg of patient’s body weight per day is administered. A number of authors use more concentrated 3-5% bicarbonate solutions in correspondingly smaller doses. Infusions are performed daily or every other day under the control of blood pressure, acid-base balance indicators determined on the Astrup apparatus, and blood electrolytes until a clinical and biochemical effect is obtained. Relative contraindications to the administration of bicarbonate are edema, heart failure, high hypertension, hypernatremia. Intravenous administration of sodium lactate is widely used to combat acidosis. In this case, the lactate ion is metabolized by the liver, and the released sodium forms bicarbonate with CO 2. Depending on the severity of the case, 10-20 ml of 1/6 M (1.8%) sodium lactate solution is administered per kg of the patient’s body weight per day. You can use a more concentrated 10% solution; lactate in a correspondingly lower dosage. Successful treatment; sodium lactate is impossible in cases of liver dysfunction, as well as in heart failure and other conditions accompanied by increased formation of lactic acid.

In case of acidosis, which occurs with a significant decrease in the level of chlorides in the plasma, exicosis, osmotic hypotension due to loss of salt, a NaCl solution is administered along with bicarbonate or lactate. The so-called physiological NaCl solution contains a significant excess of chlorine compared to the composition of the extracellular fluid. Excess chlorine displaces an equivalent amount of bicarbonates from the extracellular fluid, promoting a shift in the reaction to the acidic side. A saline solution does not contain osmotically “free” water to cover pulmonary, skin and other expenses, so the administration of NaCl saline solution is usually combined with the administration of solutions of bicarbonate, sodium lactate or 5% glucose. These solutions can be administered in various combinations. Typically, an isotonic 1.8% lactate solution or a 1.3% sodium bicarbonate solution and a physiological NaCl solution are administered in a ratio of 1: 2. In total, the solutions contain an amount of sodium and chlorine that approximately corresponds to their normal ratio in the extracellular fluid. For each liter of solution, about 20 ml of a 10% solution of calcium gluconate or CaCl 2 is injected. Infusions of glucose solutions are especially indicated for acidosis in debilitated patients. Glucose solutions, usually prescribed along with insulin, help reduce hyperkalemia, which often accompanies acidosis, and also serve as a source of “free” water. Intravenous drip infusion of 5% glucose is usually combined with the introduction of an equal amount of isotonic 1.3% sodium bicarbonate solution (1: 1). For hypersalemia, these solutions are administered in a ratio of 2: 1 or 3: 1. At the same time, patients receive calcium supplements and 8-12 units of insulin per day (1 unit of insulin per 4 g of administered sugar). Recently, buffer amines (TRIS; trisamine) have been used in the treatment of acidosis. The advantage of the latter over other alkalizing solutions is that they penetrate into cells, correcting the intracellular pH. However, experience with these substances is still insufficient. Both doses and methods of administering corrective solutions are determined individually. It should be considered erroneous to determine the dose of administered bicarbonate based on sodium deficiency, since in most cases there is no direct relationship between the degree of acidosis and the level of sodium in plasma. For acid-base balance, it is not so much the absolute level of natremia that matters, but the mutual ratios of constant bases and acids, the nature of those anions, in combination with which sodium is in the plasma and excreted in the urine. All these circumstances must be taken into account when choosing appropriate therapy for a given case. In addition to the above-mentioned approximate dosages, a number of formulas have been proposed for calculating the amount of corrective solution that needs to be administered to the patient:

1. Amount of 4-5% sodium bicarbonate solution in ml = “BE” (base deficiency determined on the Astrup apparatus, in meq/l) X body weight in kg: 2.

2. Amount of 10% sodium lactate solution in ml or 8.5% sodium bicarbonate solution in ml, or amount of sodium bicarbonate in mEq = “BE” in mEq/L X body weight in kg X 0.3.

3. The amount of sodium bicarbonate or lactate in mEq = the volume of extracellular fluid in L (20% of body weight in kg) X 2 X (25 - alkaline blood reserve in mEq / L) or X (22 - standard blood bicarbonate determined on the machine Astrup, in meq/l).

4. Amount of 0.3 M (3.6%) TRIS solution in ml = “BE” in mEq/L X body weight in kg.

In case of renal failure or oliguria, the dose of the alkalizing solution calculated using the formulas is usually administered fractionally over two days.

However, the formulas recommended by various authors for calculating the amount of injected solution should be used with caution, since they usually proceed from the value of only a few indicators that need to be taken into account. With the exception of extremely severe cases of uremic coma, one should caution against attempts to quickly correct the existing deficit. In a chronic kidney patient, a gradual, long-term correction, designed to slowly achieve normal values ​​over several days, is much more beneficial. At the same time, the danger of undesirable hemodynamic and electrolyte shifts is reduced, the body’s own compensatory mechanisms manage to become involved in the correction of existing disturbances in water-electrolyte metabolism and acid-base balance, and a gradual equalization of not only extra-, but also intracellular electrolyte balance occurs. Alkalinization therapy must be comprehensive. For moderate acidosis, along with an appropriate diet (vegetables, fruits, milk), sodium bicarbonate, lactate or sodium citrate is prescribed orally (respectively in doses of 5-10, 3-6 and 4-8 g per day). In more severe cases, alkaline intestinal and gastric lavages (0.25% NaHCO 2 solution every other day) are useful, which, along with the alkalizing effect, promote the removal of nitrogenous waste from the body, alkaline enemas. If these procedures are not able to stop acidosis, resort to intravenous (bicarbonate, sodium lactate, glucose, physiological NaCl solution) or subcutaneous (5% glucose solution, physiological NaCl solution) administration of solutions. In some cases, an alkalizing effect is observed when using diuretics, leading to the loss of chlorine and potassium, anabolic hormones, as well as when long-term treatment; renal patients with large doses of corticosteroid hormones.

Of the 22 patients with acute nephritis that we examined during treatment with large doses of prednisolone (60 mg prednisolone per day), an increase in the concentration of blood bicarbonates was observed in 21. In patients in this group, the plasma concentration of bicarbonates normalized as a result of treatment. A less pronounced and less persistent increase in the concentration of blood bicarbonates was observed in the group of patients with chronic glomerulonephritis (23 people) who received the same hormonal therapy. In the control group of patients with acute and chronic glomerulonephritis who received symptomatic treatment, the correction of acidosis was much less pronounced. In the corrective effect of corticosteroid hormones on renal acidosis, stimulation of the acid-secreting function of the kidneys (Fig. 69) and electrolyte changes (sodium retention observed in some cases, loss of intracellular potassium with the development of extracellular alkalosis) are important.

Rice. 69. Increased acid-excretion function of the kidneys in patients with chronic glomerulonephritis under the influence of symptomatic and corticosteroid therapy.
Columns: oblique shading - patients receiving corticosteroids; light - those receiving symptomatic treatment.

In extremely severe patients with oligoanuria, acidosis can be corrected using hemodialysis (artificial kidney). Only dialysis can remove the excess hydrogen ions constantly formed in the body in such patients. At the same time, during the process of hemodialysis, the blood buffer systems are restored due to bicarbonate ions, and, in contrast to the intravenous administration of alkaline solutions, without the simultaneous administration of excess sodium. If the partial pressure of CO 2 in the blood of patients during hemodialysis remains low, the initial metabolic acidosis by the end of dialysis can turn into respiratory alkalosis (Blumentals et al., 1965). Correction of acidosis is much less successful in cases where hemodialysis is accompanied by pyrogenic reactions, and also if the acidosis, along with the metabolic one, has a respiratory component (Sanchez Sicilia, Kolff, 1964).It should be emphasized that during hemodialysis, ion exchange occurs not only between the plasma and the dialysate solution. At a certain stage, intracellular and interstitial fluid are included in the exchange, which in some cases makes the task of correcting acidosis even more difficult (A. A. Chervinsky, 1966). A number of authors note the successful correction of renal acidosis during peritoneal dialysis. Good results were obtained with recirculating peritoneal dialysis (G. Ya. Alapin et al., 1967), as well as when alternating hemo- and peritoneal dialysis (A. Ya. Pytel, I. N. Kuchinsky, 1967).

We studied the dynamics of acid-base balance in 21 patients with chronic renal failure, in whose treatment peritoneal dialysis was used. While in control group patients with renal failure who received symptomatic treatment, acid-base balance indicators tended to progressively decrease, in patients treated with peritoneal dialysis, these indicators were able to stabilize at subnormal values ​​for some time. Normalization of acid-base balance was observed only in individual patients and was short-term. In general, the correction of acidosis with peritoneal dialysis was significantly worse than with hemodialysis or intravenous administration of alkalizing solutions. Poor correction of acidosis in some cases of peritoneal dialysis may be associated with increased catabolism as a result of surgery (fistula), infection, temporary decrease in diuresis and acid-excreting function of the kidneys. Therapy in these cases should be comprehensive. Thus, we combine peritoneal dialysis with intravenous correction, administration of anabolic hormones, active antibacterial therapy and so on.

There are some indications in the literature about the gradual normalization of acid-base balance after a successful kidney transplant.

Effective and timely correction of acidosis in kidney disease sometimes contributes to a more or less long-term remission.

The concept of CKD has been used relatively recently by nephrologists and doctors of other specialties. Chronic kidney disease is characterized by the presence of morphological or functional disorders in the work of the organ.

Doctors of various specialties know what CKD is, but nephrologists and cardiologists, as well as urologists, are more likely to encounter this supernosological concept.

Chronic kidney disease is a serious pathology, which in the future, if not properly treated, will lead to severe renal failure. Ultimately, the patient will undergo hemodialysis or a kidney transplant.

The definition of the concept was introduced back in 2000 by the US National Kidney Foundation. The Working Group on Improving Outcomes in Kidney Disease has also made efforts to create a working classification.

Chronic renal failure does not include anatomical changes in the structure of the kidneys that appear as a result of or against the background of pathologies of the urinary system. It only reflects a violation of nitrogen excretion and other functions of the organ.

In this context, chronic kidney disease is a broader term. It is not for nothing that CKD is classified as a supranosological concept.

CKD is not considered separate disease. This is more an indication for the patient and the doctor that there is a violation of the function or structure of the kidneys, which means that action is needed to treat and prevent the progression of the pathology.

The formation of CKD is based on diseases of the glomerular apparatus or renal parenchyma. But pathologies of all organs and systems can lead to impaired renal function. Thus, cardiologists talk about cardiovascular disorders, warning that heart failure and renal failure develop and progress in parallel.

According to the generally accepted definition, CKD includes any conditions accompanied by impaired renal function, lasting three or more months, as well as clinical manifestations with morphological signs of kidney damage.

Formulating a diagnosis requires calculating the glomerular filtration rate. First, indicate the degree or stage of CKD. Then, in parentheses, it is necessary to confirm this by calculating the GFR according to one of known formulas(e.g. CKD-EPI or Cockcroft-Gault).

Classification and stages of CKD

The main classification criterion for determining the degree of chronic kidney disease is the glomerular filtration rate. This option is functional. It is difficult to determine at this stage using laboratory or other objective research methods. Therefore, they resort to using calculation formulas.

The most popular is CKD-EPI. The stage of CKD depends on GFR. The calculation using the formula can be done using a special calculator, which can be found on the Internet. Depending on the indicator, CKD is classified into stages.

The rate of glomerular filtration depends on many parameters. These include a person’s body weight, height indicator, as well as gender and age. All these parameters are included in the electronic formula for calculating GFR.

To determine the glomerular filtration rate using this formula, you also need to know another important indicator - serum creatinine. It is determined during a biochemical blood test. It is measured in micromoles per liter.

The more patient parameters, the more accurately the glomerular filtration rate can be determined. Stage is determined by creatinine level and GFR.

Stages of the disease

The classification of CKD includes 5 stages. Among them, CKD in phase 3 is divided into two periods – C3a and C3b. The main criterion is the glomerular filtration rate at a certain stage of chronic renal failure.

In stage 1 CKD, GFR exceeds 90 ml/min/1.73 m². But there are signs of kidney damage. Most often this is hypertension or diabetes with changes in the urine. In stage 2 CKD, GFR varies from 60 to 89. The development of chronic kidney disease is accompanied by a steady decrease in glomerular filtration rate without adequate treatment.

Further, the disease of the urinary system progresses. This affects the function and functioning of the kidneys. Therefore, stage 3 CKD is characterized by an even more pronounced decrease in glomerular filtration rate.

In CKD C3a, GFR ranges from 45 to 60, while for chronic kidney disease stage C3b it is characterized by a decrease to 30 ml/min/1.72 m². The nephrologist requires decisive measures for treatment and prevention.

In stage 4 CKD, preparations are being made for dialysis. The GFR level reaches 15 ml/min. This value is borderline. GFR below 15 ml/min/1.72 m² – grounds for the diagnosis of “terminal kidney disease” – CKD stage 5.

Causes

The main etiological factors underlying renal failure are diseases of the urinary system.

The most common pathology is pyelonephritis. This is about inflammatory disease, striking renal parenchyma and the collecting system. Chronic pyelonephritis implies the persistence of an infectious agent in the urinary tract and kidneys. In the absence of proper treatment, renal dysfunction progresses with a gradual decrease in glomerular filtration rate.

Causes of chronic renal failure include glomerulopathies. This is a group of diseases in which the glomerular apparatus is primarily damaged. These include:

• poststreptococcal glomerulonephritis;
• diabetic nephropathy;
• gouty kidney disease;
• ANCA glomerulonephritis;
• glomerulopathies associated with connective tissue disease.

With these pathologies, the filtration process is disrupted. Without treatment, all kidney functions are impaired, and CKD increases. The concentration of creatinine and other nitrogenous compounds in the blood increases. Glomerular filtration rate decreases, chronic kidney disease progresses.

Risk factors for the development of kidney disease and CKD include high blood pressure, frequent genitourinary infections, diabetes mellitus, pregnancy, early onset of sexual activity and frequent changes of sexual partners.

Particular attention is paid to hypertension. According to modern cardiological recommendations, there is a whole section in the treatment hypertension, dedicated to nephroprotection. Cardiologists and therapists must calculate the glomerular filtration rate and give appropriate recommendations so that the disease does not progress.

Diabetic nephropathy is a common complication of diabetes. If blood glucose levels are not controlled, the likelihood of kidney damage increases significantly. Glomerular filtration rate decreases rapidly and chronic kidney disease progresses.

Symptoms

Signs of chronic kidney disease are nonspecific. Manifestations of CKD in grades 1 and 2 can be masked by the underlying disease.

In chronic pyelonephritis, pain in the lower back of a pulling or aching nature is bothersome. Periodically, the patient complains of urinary disorders. As the infection worsens, you may experience a burning or stinging sensation when emptying your bladder.

Glomerulopathy is accompanied by hypertensive and edematous syndrome. The pressure increases sharply, while the diastolic pressure changes to a greater extent, decreases pulse pressure. Swelling appears on the face, in the periorbital area.

Then patients notice some puffiness of the face. When the disease is uncontrolled, swelling spreads to the limbs. At first, rings are not put on the fingers. Then difficulties arise with shoes due to severe swelling of the legs and feet. While taking diuretics, excess fluid is eliminated.

Symptoms of uremia appear in the later stages of CKD (less often with C3, more often with C4, C5). At stage 5, extrarenal blood purification is already necessary. With uremia, the following complaints are possible:

• severe weakness;
• prostration;
• unmotivated fatigue;
• decreased appetite;
• irritability, emotional lability;
• asthenization;
• headache;
• increased heart rate;
• abdominal pain (caused by the effect of nitrogenous compounds on the mucous membrane of the stomach and intestines with the development of gastritis, colitis and enterocolitis);
• decrease in the volume of urine excreted (oliguria, up to anuria);
• breathing disorders such as shortness of breath;
• swelling;
• increased blood pressure.

Chronic kidney disease in its later stages is difficult to treat. Taking medications is unlikely to help restore kidney function. But it is possible to slow down the progression of the disease.

Diagnosis of the disease

First of all, to make a correct diagnosis, it is necessary to carefully collect complaints and anamnesis. It is important to understand what pathology caused a disease such as chronic kidney disease.

The next stage after clarifying complaints, collecting anamnesis of life and illness is an objective study. The specialist evaluates the patient’s condition holistically and for each organ system.

With chronic kidney disease, the color of the skin changes, its moisture content and turgor decrease. The skin color is usually pale or yellowish-sallow. Pallor is caused by a violation of the synthesis of erythropoietin, which is produced by kidney cells. It is usually observed in the later stages of the disease.

The sallow color of the skin is explained by the deposition of pigments involved in bilirubin metabolism - urochromes. In CKD and chronic renal failure, the excretion of nitrogenous compounds, including urea, is reduced. In case of insufficient renal function, this metabolite is excreted through the lungs, gastrointestinal tract, and skin. This gives it a powdery look. The skin becomes very dry.

CKD is a cause of fluid and electrolyte disturbances. In the initial stages, sodium is lost. The patient is worried about thirst. He feels weak. The skin becomes dry, turgor decreases. When measuring blood pressure, a tendency towards hypotension is noted.

On the contrary, in the final stages of the disease, sodium is retained. At the same time, pressure increases and excess fluid accumulates in tissues and organs. The patient is swelling. His shortness of breath is increasing due to stagnation in the pulmonary circulation.

With uremia, the doctor sees that the patient is suffering from shortness of breath. It is of a mixed nature. Uremic gastritis is manifested by abdominal pain in the projection of the epigastrium.

Upon palpation of this area it is diagnosed increased sensitivity or soreness. Uremic colitis is accompanied by pain along the intestines. Pathological impurities may appear in the stool.

Laboratory and instrumental methods in the diagnosis of CKD

If there is any suspicion of kidney disease, general clinical tests are prescribed. This is a blood and urine test. In the blood, the doctor will be interested in the level of leukocytes, red blood cells, hemoglobin and erythrocyte sedimentation rate (ESR).

Leukocytosis (an increase in the number of white blood cells) will indicate the presence of pyelonephritis. Anemia, characterized by a decrease in the level of hemoglobin or red blood cells, develops in stages C3-C5 of kidney disease.

A general urine test is intended to help the clinician decide on further research. Leukocyturia dictates the need for bacteriological culture. Changes in urine parameters should be confirmed by Nechiporenko's test. It more reliably shows the cellular composition and allows for a preliminary differential diagnosis.

Determination of proteins in urine can be quantitative or qualitative. The second method is most often used. In the general analysis, the degree of proteinuria is indicated in crosses: the more of them, the more protein in the urine. In diabetes mellitus, the presence of microalbumin should also be determined. This is a very specific test for early diagnosis of the most initial stages kidney damage or dysfunction.

Other important urine indicators include glucose, urobilin, and urine acetone. But it is impossible to judge the presence of CKD from them. These parameters only indicate the cause of primary kidney damage.

A biochemical blood test is of interest to doctors in terms of calculating the glomerular filtration rate. Depending on the serum creatinine concentration, it may be low or increased rate SCF. It is described above how to use formulas to calculate it.

Renal function is also assessed using the Zimnitsky test. A decrease or loss of the organ’s concentrating ability is diagnosed.

Imaging techniques (ultrasound, radiography, tomography) are designed to identify primary kidney disease.

Treatment

1. Treatment of the underlying pathology that led to impaired renal function.
2. Slowing the progression of CKD.
3. Prevention of cardiovascular complications.
4. Deciding on the advisability of dialysis therapy and preparing for it.
5. Treatment includes drug and non-drug treatments. The basis of the regime renal pathology– compliance with dietary recommendations. They depend on the degree and type of water and electrolyte disturbances. For chronic kidney disease in the early stages, table No. 7 according to Pevzner is recommended.
6. The consumption of protein and table salt is limited. This is important when kidney function insufficiency increases.

Chronic renal failure occurs with impaired excretion of sodium, potassium, and phosphorus. The intake of these electrolytes from food is limited as much as possible. Dairy products, fish, and jellied meat are prohibited.

Salt should not be added to prepared food. It is added only during heat treatment. The maximum allowable daily amount of table salt for chronic kidney disease is 1.5-3.0 grams. Exceeding this norm will lead to worsening hypertension syndrome.

Close attention is paid to the volume of fluid consumed. It should exceed by half a liter the amount that is excreted from the body daily. The exception is situations with cardiac decompensation.

Considering that the process of excretion through the kidneys is disrupted, it is necessary to create all the conditions to normalize the functioning of the digestive tract. It is necessary to achieve daily bowel movements and eliminate constipation.

The diet for the treatment of stage 4 or terminal stage CKD on the background of hemodialysis or peritoneal dialysis does not imply significant restrictions in food and water intake. The diet must be complete and contain the required amount of vitamins and microelements.

Principles of drug treatment

In the early stages of CKD, protective treatment is prescribed. This is what doctors do primary care– therapists, general practitioners, as well as cardiologists and endocrinologists.

In the first two stages, the patient has a certain kidney disease with or without dysfunction.

The essence of treatment is nephroprotection. This is a prophylactic prescription of drugs that prevent the progression of pathology and improve the functioning of nephrons. For maximum nephroprotective effect, drugs from the group of blockers of the renin-angiotensin-aldosterone system are used.

Showed their best side ACE inhibitors and angiotensin receptor blockers. The dosage depends on the initial blood pressure level and the presence of concomitant vascular pathology.

In the third stage and later, the patient should be treated by a nephrologist. Drugs are prescribed to reduce the degree of uremia.

Under stationary conditions, this is sodium bicarbonate. Therapy is aimed at limiting the intake of nephrotoxic drugs. Another important area is constant monitoring of nitrogen metabolism indicators.

Anemia is treated with iron supplements. If ineffective, erythropoietins are indicated. Only a nephrologist at the regional level or a city nephrocenter has the right to prescribe them.

Diagnostic signs of stages C4 and C5 should be the reason to begin preparing for dialysis. Possible methods of therapy are discussed, conversations are held with the patient and relatives.

Forecast

Living with a chronic disease is a difficult experience for both the patient and his family. Therefore, in the first stages you will need the help of a psychotherapist.

The prognosis of chronic kidney disease depends on many factors:

• patient's age;
• the presence of concomitant aggravating pathology;
• general condition of the patient;
• timeliness of treatment.

Other diseases that affect the condition of the kidneys in one way or another are also taken into account. These are liver and cardiovascular diseases, poisoning, systemic pathologies.

If nephroprotective treatment is started in a timely manner, the patient is registered with a nephrologist in the nephrocenter and is constantly monitored there, he has a chance to live a long and happy life.

The patient must listen to what is happening in his body and consult a doctor in time. If the disease is detected in the final stages, the prognosis is questionable. But dialysis and kidney transplantation are the way out of this difficult situation.

Modern methods of treating chronic renal failure
Modern methods of treating chronic renal failure

CHRONIC RENAL FAILURE

Until recently, chronic renal failure (CRF) was defined as a clinical and biochemical syndrome that occurs with kidney damage of any etiology, caused by a gradually progressive loss of excretory and endocrine functions of the organ due to the irreversible loss of functioning nephrons.
In this case, unlike acute renal failure, the pathophysiological processes are irreversible, which lead to these disorders. Their development only partially depends on the etiology of the underlying renal disease, since the leading pathogenetic mechanisms of damage to functioning nephrons in this situation are intraglomerular hypertension, hyperfiltration in the glomerulus and the nephrotoxic effect of proteinuria (more precisely, disorders of renal protein transport).
The discovery of the unity of the mechanisms of pathogenesis of kidney tissue damage in chronic diseases of this organ was one of the important factors that led to the creation of a fundamentally new concept - chronic kidney disease (CKD).
Reasons for the emergence of the concept of CKD.
Currently, there is a dramatic increase in the number of patients with chronic renal pathology.
This is primarily determined by the increase in the incidence of diabetes mellitus, the aging of the population and, accordingly, the increase in the number of patients with kidney damage of a vascular nature.

The progressive increase in the number of such patients is regarded as a pandemic. The above factors have led to a catastrophic increase in the number of people who require renal replacement therapy (RRT) - various types of dialysis or kidney transplantation.
The long-standing approach to secondary prevention of end-stage renal disease (ESRD) has also contributed to the increase in the number of patients on RRT.

When a certain degree of decline in renal function was achieved, it was not considered necessary to resort to any special methods to slow the progression of the pathological process in the renal tissue.
In addition, over the past decades, the quality of RRT technologies has continuously improved, which has caused a sharp increase in life expectancy for patients receiving such treatments.

All this has led to an increased need for dialysis beds, organ transplants and rising costs.
Already in the sixties of the last century, it became clear that many mechanisms of progression of chronic kidney diseases are quite universal and largely operate regardless of etiology. Equally important was the identification of risk factors for the development and progression of a chronic pathological process in renal tissue.
Like the mechanisms of progression, they turned out to be basically the same in various chronic kidney diseases and quite similar to cardiovascular risk factors.

Clarification of the pathogenetic mechanisms of progression of chronic kidney diseases, identification of risk factors for their occurrence and development has made it possible to develop well-founded treatment regimens that can actually delay the onset of RRT or reduce the number of lethal complications.
Approaches to renoprotection for various diseases kidneys were basically identical (angiotensin-converting enzyme inhibitors, angiotensin II AT1 receptor antagonists, non-dihydropyridine calcium channel blockers, low-protein diet).
All of the above required rethinking, primarily to develop effective measures to further improve medical and social care for patients with chronic kidney disease.
One of the prerequisites for this should be unity or at least similarity of criteria for identifying, describing, assessing the severity and rate of progression of renal pathology.
However, there was no such unity among nephrologists. For example, in the English-language literature one could find about one and a half dozen terms used to designate conditions associated with the appearance of chronic renal dysfunction.

It should be noted that in domestic nephrology the terminological problem was less acute. The phrase “chronic renal failure” (CRF) or, in appropriate cases, “end-stage renal failure”, “end-stage chronic renal failure”, etc. was usually used.
However, there was no common understanding of the criteria for chronic renal failure and assessment of its severity.

Obviously, the adoption of the concept of CKD should sharply limit the use of the term “chronic renal failure”.

In the NKF classification, the phrase “renal failure” remains only as a synonym for stage V. CKD.
At the same time, in the English-language nephrological literature, the name “end-stage renal disease” has become widespread.
The developers at NKF thought it would be appropriate to retain the use of this term since it is widely used in the United States and refers to patients who are receiving therapy various methods dialysis or transplantation, regardless of the level of kidney function.
Apparently, in domestic nephrological practice it is worth preserving the concept of “end-stage renal failure”. It is advisable to include patients, both already receiving RRT, and patients with stage V CKD, for whom replacement treatment has not yet been started or for whom it is not carried out due to organizational problems.
Definition and classification of CKD.
A number of issues briefly mentioned above have been addressed by the National Kidney Foundation (NKF). The Foundation created a group of experts who, as a result of analyzing many publications on diagnostics and treatment, assessing the significance of a number of indicators in determining the rate of progression of kidney diseases, terminological concepts and agreements with administration representatives, proposed the concept of chronic kidney disease (CKD). ).

When developing the concept of CKD, the experts of the NKF working group pursued several goals: Definition of the concept of CKD and its stages, regardless of the cause (etiology) of renal failure (disease).
Selection of laboratory parameters (research methods) that adequately characterize the course of CKD.
Determination (study) of the relationship between the degree of renal dysfunction and complications of CKD.
Stratification of risk factors for the progression of CKD and the occurrence of cardiovascular diseases.

NKF experts proposed a definition of CKD, which is based on a number of criteria:
Kidney damage lasting > 3 months, which manifests itself as structural or functional impairment of the organ with or without a decrease in GFR.
These damages are manifested either by pathomorphological changes in the renal tissue, or by changes in the composition of the blood or urine, as well as changes when using methods of visualization of the structure of the kidneys GFR< 60 мл/мин/1,73 м2 в течение трех и более месяцев, при наличии или отсутствии других признаков повреждения почек.
In other words, chronic kidney disease can be defined as “the presence of kidney damage or decreased levels of kidney function for three months or more, regardless of diagnosis.”

NKF experts have identified five stages of CKD depending on the severity of the decrease in GFR

Let us again draw attention to a very important point.
In the classification, risk factors for the development and progression of CKD are highlighted in a separate line.
One of the most important among them is the systemic arterial hypertension or proteinuria.
It should be borne in mind that, according to the conclusion of NKF experts, the presence of risk factors alone does not provide grounds for making a diagnosis of CKD, but requires a certain set of preventive measures).

The concept of CKD, which is not directly related to a nosological diagnosis, does not negate the nosological approach to the diagnosis of a specific kidney disease.
However, it is not a purely mechanical combination of chronic kidney damage of various natures.
As noted earlier, the development of this concept is based on the unity of the leading pathogenetic mechanisms of progression of the pathological process in renal tissue, the commonality of many risk factors for the development and progression of kidney diseases and the resulting similarity in methods of therapy, primary and secondary prevention.

In this sense, CKD is close to the concept of coronary heart disease (CHD).
The term CKD, as soon as it appeared, won citizenship rights not only in the United States, but also in many other countries.
The VI Congress of the Scientific Society of Nephrologists of Russia, held on November 14-17, 2005 in Moscow, clearly supported the need for widespread introduction of the concept of CKD into the practice of domestic healthcare.

General clinical manifestations of late stages of CKD.
Signs associated with the development of renal dysfunction and little dependent on the underlying pathological process in the kidneys usually begin to appear at the third stage of CKD and reach maximum severity by the fifth. At first, moderate polyuria, nocturia, decreased appetite, and a tendency to anemia are usually recorded.

A drop in GFR below 30% of the normal level leads to the appearance of symptoms of uremic intoxication, an increase in hyporegenerative anemia (due to a decrease in erythropoietin production), disturbances in phosphorus-calcium metabolism and the formation of symptoms of secondary hyperparathyroidism (due to a decrease in the intrarenal synthesis of the active metabolite of vitamin D-1, 25(OH)2D3; synonyms: 1,25-dihydroxy-cholecalciferol, calcitriol, D-hormone, etc.), metabolic acidosis (due to a decrease in renal excretion of hydrogen ions and suppression of bicarbonate ion reabsorption).

Compensation for metabolic acidosis is carried out by the lungs by increasing alveolar ventilation, which leads to the appearance of deep, noisy breathing. Secondary hyperparathyroidism, along with acidosis, leads to the development of osteodystrophy, which can manifest itself as pathological fractures. In addition, disturbances in calcium-phosphorus homeostasis often cause the appearance of extraosseous calcifications, including vascular calcification. Secondary hyperparathyroidism, skeletal damage, and soft tissue calcification are most severe in patients receiving RRT and represent a very serious clinical problem in these patients.
As CKD progresses, patients develop hemocoagulation disorders, which is accompanied by the slight formation of subcutaneous hematomas and increased risk development of bleeding, including gastrointestinal.

The skin is dry ("brights don't sweat"), and many patients experience painful itching, leading to scratching.
The initially present polyuria can be replaced by oliguria, leading to overhydration and swelling of the internal organs, including edema of the lungs and brain.
In the later stages of CKD, uremic polyserositis can develop, in particular uremic pericarditis, which is a poor prognostic sign and requires immediate initiation of RRT.

Sometimes the so-called "terminal nephrotic syndrome».
General cerebral symptoms gradually increase: lethargy, drowsiness, apathy, and sometimes sleep rhythm disturbances.
Almost all patients are characterized by uremic dyslipoproteinemia, leading to acceleration of atherogenesis processes and increased cardiovascular risks.

Diagnostics. Provided early detection of the underlying renal pathological process (GN, secondary nephropathies, diabetic nephropathy, etc.) and follow-up of the patient, diagnosis usually does not cause difficulties. To monitor renal function in practical work, the level of plasma creatinine and GFR are monitored over time.
Some diagnostic difficulties may arise when managing patients in whom azotemia is detected for the first time. In these cases it may become topical issue distinguishing between acute and chronic renal failure.

Now a little mathematics, which, unfortunately, cannot be done without in this section.
The problem of estimating glomerular filtration rate in practical medicine. Glomerular ultrafiltration is the initial and main mechanism of urine formation.
The way the kidneys perform all their diverse functions depends decisively on its condition.
It is not surprising that members of the NKF working group chose glomerular filtration rate (GFR) not only as the main criterion for distinguishing specific stages of CKD, but also as one of the most important basis for making a diagnosis of chronic kidney disease. The developers of the National Kidney Foundation have convincingly shown that the degree of decline in GFR is very closely associated with other clinical or metabolic changes that occur as chronic nephropathies progress.

It is clear that the introduction of the concept of CKD requires the availability of a reliable, simple and inexpensive method of measuring GFR in clinical practice.

To date, a very large number of methods and their modifications have been developed that make it possible to estimate GFR with varying degrees of accuracy. However, their use in widespread clinical practice is limited by complexity and high cost.
Therefore, they are usually used for specific research purposes.

Throughout the world in practical medicine, the main estimates of GFR until recently remained the serum creatinine concentration (Cgr) or endogenous creatinine clearance (Ccreatinine clearance).
Both of these methods have a number of significant disadvantages. Serum creatinine concentration as an index of GFR.

Creatinine is a low molecular weight product of nitrogen metabolism.
It is mainly excreted by the kidneys by glomerular filtration, although some is secreted in the proximal tubules. In streets with unimpaired filtration capacity, the proportion of creatinine secreted by the tubules is small. However, the contribution of tubular secretion to the distortion of estimates of glomerular filtration rate may increase sharply with a decrease in renal function.

The process of creatinine formation in healthy people occurs almost immediately constant speed.
This determines the relative stability of Cgr.
Despite the relative stability of creatinine production, there are a significant number of reasons, including those not directly related to the functional state of the kidneys, that can affect the level of Cgr. The main determinant of serum creatinine levels.
apparently, is the volume of muscle mass, since the production of this metabolite is proportional to this volume.
An important factor influencing serum creatinine levels is age.
GFR in adults declines progressively after age 40.
Decreased creatinine generation caused by age naturally increases GFR levels. Sgr in women is usually slightly lower than in men. The main significance in the appearance of these differences, apparently, is also associated with lower muscle mass in females.
Thus, clinical assessment of GFR based on serum creatinine levels cannot be carried out without taking into account the anthropometric, gender and age characteristics of the patient.

Under conditions of pathology, including kidney pathology, all factors that determine the level of serum creatinine can be modified to one degree or another.
The available information does not make it possible to come to a final conclusion about whether creatinine formation is increased, unchanged, or decreased in patients with chronic kidney disease.

However, when GFR decreases to 25-50 ml/min, patients usually spontaneously reduce protein intake (nausea, vomiting, anorexia).
Serum creatinine levels may be affected by the intake of various medicines.
Some of them (amnoglycosides, cyclosporine A, platinum preparations, X-ray contrast agents, etc.) are nephrotoxic drugs, when prescribed, an increase in Cg reflects a real decrease in GFR.
Others are capable of undergoing the Jaffe reaction.
Finally, some drugs selectively block proximal tubular creatinine secretion without any significant effect on GFR.
Cimetidine, trimethoprim and, possibly, to some extent phenacetamide, salicylates and vitamin D3 derivatives have this property.

The determined value of creatinine concentration in blood serum depends quite significantly on the analytical methods used to measure this indicator. Until now, the level of creatinine in biological fluids is most often assessed using the Jaffe reaction.
The main disadvantage of this reaction is its low specificity.
This reaction can involve, for example, ketones and keto acids, ascorbic and uric acid, some proteins, bilirubin, etc. (“non-creatinine chromogens”). The same applies to some cephalosporins, diuretics, if they are prescribed in high doses, phenacetamide, acetohexamide and methyldopa (when administered parenterally). At normal values serum creatinine, the contribution of non-creatinine chromogens to its total concentration can range from 5 to 20%.

As kidney function declines, serum creatinine concentrations naturally rise.
But this increase is not accompanied by a proportional increase in the level of non-creatinine chromogens.
Therefore, their relative contribution to the concentration of total chromogen (creatinine) in the serum decreases and usually in this situation does not exceed 5%. In any case, it is clear that creatinine levels measured using the Jaffe reaction will underestimate the true GFR values.
Rapid changes in the latter parameter also lead to disruptions in the clarity of the inverse relationship between the concentration of serum creatinine and GFR.
In relation to them, the increase or decrease in Cgr may be delayed by several days.
Therefore, special care must be taken when using Cgr as a measure functional state kidneys during the development and resolution of acute renal failure.
Use of creatinine clearance as a quantitative measure of GFR. The use of SSG compared to Sgr provides one significant advantage.
It allows you to obtain an estimate of the glomerular filtration rate, expressed as a numerical value with a dimension corresponding to the nature of the process (usually ml/min).

However, this method of assessing GFR does not resolve many issues.
Obviously, the accuracy of the measurement of CVg largely depends on the correctness of urine collection.
Unfortunately, in practice, the conditions for determining the volume of diuresis are often violated, which can lead to either overestimation or underestimation of Cg values.
There are also categories of patients in whom quantitative urine collection is almost impossible.
Finally, when assessing the GFR value great value has the magnitude of tubular secretion of creatinine.
As noted above, in healthy people the proportion of this compound secreted by the tubules is relatively small. However, under conditions of kidney pathology, the secretory activity of proximal tubular epithelial cells in relation to creatinine can sharply increase.

However, in a number of individuals, including those with a significant decrease in GFR, creatinine secretion may even have negative values. This suggests that they actually have tubular reabsorption of this metabolite.
Unfortunately, it is impossible to predict the contribution of tubular secretion/reabsorption of creatinine to the error in determining GFR based on CFR in a particular patient without measuring GFR using reference methods. “Calculation” methods for determining GFR.

The very fact of the presence of an inverse, although not direct, relationship between Cgr and GFR suggests the possibility of obtaining an estimate of the glomerular filtration rate in quantitative terms based only on the concentration of serum creatinine.

Many equations have been developed to predict GFR values ​​based on Cgr.
Nevertheless, in real practice of “adult” nephrology, the Cockcroft-Gault and MDRD formulas are most widely used.

Based on the results of the multicenter study MDRD (Modified of Diet in Renal Disease), a series of empirical formulas were developed that make it possible to predict GFR values ​​based on a number of simple indicators. The best agreement between the calculated GFR values ​​and the true values ​​of this parameter, measured by the clearance of 125I-iothalamate, was shown by the seventh version of the equations:

However, it should be borne in mind that there are situations where “calculated” methods for determining GFR are unacceptable.

In such cases, at least a standard creatinine clearance measurement should be used.
Situations in which it is necessary to use clearance methods for determining GFR: Very elderly age. Non-standard body sizes (patients with limb amputations). Severe emaciation and obesity. Diseases of skeletal muscles. Paraplegia and quadriplegia. Vegetarian diet. Rapid decline in kidney function.
Before prescribing nephrotoxic drugs.
When deciding whether to start renal replacement therapy.
It must also be remembered that the Cockcroft-Gault and MDRD formulas are not applicable in children.

Cases of acute deterioration of renal function in patients with pre-existing chronic kidney pathology, the so-called “acute on chronic renal failure”, or, in the terminology of foreign authors, “acute on chronic renal failure” deserve special attention.
From a practical point of view, it is important to emphasize that timely elimination or prevention of factors leading to acute impairment of kidney function in patients with CKD can slow the rate of progression of deterioration of organ function.

The causes of acute renal dysfunction in patients with CKD may be: dehydration (limited fluid intake, uncontrolled use of diuretics); CH; uncontrolled hypertension; the use of ACE inhibitors in patients with bilateral renal artery stenosis; obstruction and/or urinary tract infection; systemic infections (sepsis, bacterial endocarditis, etc.); nephrotoxic drugs: NSAIDs, antibiotics (aminoglycosides, rifampicin, etc.), thiazides, radiocontrast agents.
It should also be mentioned that patients with CKD are especially sensitive to any potentially nephrotoxic factors, and therefore the problems of iatrogenicity and self-medication (herbs, sauna, etc.) in these cases should be given Special attention.

To others important indicator rate of progression of CKD is proteinuria.
In an outpatient setting, to assess it, it is recommended to calculate the protein/creatinine ratio in the morning urine, which is almost equivalent to measuring daily protein excretion.
An increase in daily proteinuria always means an acceleration in the rate of progression of CKD.

Treatment. Dietary recommendations.
The basic principles of the diet for CKD come down to the following recommendations:
1. Moderate limitation of NaCl consumption depending on the level of blood pressure, diuresis and fluid retention in the body.
2. The maximum possible fluid intake depending on diuresis, under the control of body weight.
3. Limiting protein intake (low-protein diet).
4. Limit foods rich in phosphorus and/or potassium.
5. Maintaining the energy value of the diet at the level of 35 kcal/kg body weight/day.
Taking into account the fact that as tubulointerstitial sclerosis develops, the ability of the kidneys to reabsorb Na may decrease, in some cases the salt regime must be expanded to 8 or even 10 g of salt per day. This is especially true for patients with the so-called “salt-losing kidney.”
In any situation, it is necessary to take into account the concomitant use of diuretics and their dose.
In a number of patients taking loop diuretics in large doses (over 80-100 mg/day of furosemide), restrictions on the consumption of table salt with food are not required.
The most adequate method of monitoring NaCl intake is daily urinary Na excretion.
A healthy person excretes at least 600 milliosmoles (mosm) of osmotically active substances (OAS) per day.
Intact kidneys are capable of significantly concentrating urine, and the total concentration of OAS (osmolality) in urine can be more than four times higher than the osmolality of blood plasma (1200 or more and 285-295 mOsm/kg H2O, respectively).
The kidneys cannot eliminate OAS (mainly urea and salts) without excreting water.
Therefore, a healthy individual is theoretically capable of excreting 600 mol in 0.5 liters of urine.

With the progression of CKD, the concentrating ability of the kidneys steadily decreases, the osmolality of urine approaches the osmolality of blood plasma and amounts to 300-400 mOsm/kg H20 (isosthenuria).

Since in the advanced stages of CKD the total excretion of OAV does not change, it is easy to calculate that to excrete the same 600 my OAV, the volume of diuresis should be 1.5-2 l/day.
This makes it clear that polyuria and nocturia appear; ultimately, limiting fluid intake in such patients accelerates the progression of CKD.

However, it should also be taken into account that with CKD stages III-V. The ability to excrete osmotically free water is gradually impaired, especially if the patient takes diuretics.
Therefore, fluid overload is fraught with the development of symptomatic hyponatremia.

Guided by the above principles, it is permissible to allow patients a free water regime, taking into account self-monitoring of daily diuresis, adjusted for extrarenal fluid losses (300-500 ml/day). Regular monitoring of body weight, blood pressure, clinical signs of overhydration, determination of daily Na excretion in urine and periodic testing of Na levels in the blood (hyponatremia!) are also necessary.

For many decades, in practical nephrology there has been a recommendation to limit the intake of proteins with food, which is based on a number of theoretical premises.
However, only recently has it been proven that a low protein diet (LPD) reduces the rate of progression of CKD.

Adaptive mechanisms of MBD in patients with CKD include: improvement of intraglomerular hemodynamics; limiting hypertrophy of the kidneys and glomeruli; positive effect on dyslipoproteinemia, effect on renal metabolism, limitation of O2 consumption by renal tissue; reduction in oxidant production; effects on T cell function; suppression of AN and transforming growth factor b, limiting the development of acidosis.
MBD is usually prescribed to patients starting from stage III. CKD.
At II st. A diet with a protein content of 0.8 g/kg body weight/day is advisable.

The standard MBD involves limiting protein intake to 0.6 g/kg/day.
In order to enrich the diet with essential amino acids, a low-protein diet can be prescribed with supplements.
Low protein diet options:
- standard MBD - protein 0.6 g/kg/day (again, regular food);
- MBD, supplemented with a mixture of essential amino acids and their keto analogues (preparation “Ketosteril”, Fresenius Kabi, Germany); food protein 0.4 g/kg/day + 0.2 g/kg/day ketosteril;
- MBD supplemented with soy proteins, protein 0.4 g/kg/day + 0.2 g/kg/day soy isolate, for example “Supro-760” (USA).

As mentioned above, when using MBD it is very important to maintain normal energy value diet due to carbohydrates and fats at a level of 35 kcal/kg/day, since otherwise the body’s own proteins will be used as energy material.
In practical work, the issue of monitoring patient compliance with the MBD is essential.

The amount of protein consumed per day can be determined based on the concentration of urea in the urine and knowing the amount of daily diuresis using the modified Maroni formula:
PB = 6.25 x EMM + (0.031 x BMI) + *SP x 1.25
where PB is protein consumption, g/day,
EMM - urea excretion in urine, g/day,
BMI - ideal body weight (height, cm - 100),
*SP - daily proteinuria, g/day (this term is entered into the equation if SP exceeds 5.0 g/day).
In this case, the daily excretion of urea can be calculated based on the volume of daily urine and the concentration of urea in the urine, which in the practice of Russian clinical laboratory diagnostics is usually determined in mmol/l:
EMM = Uur x D/2.14
where Uur is the concentration of urea in daily urine, mmol/l;
D - daily diuresis, l.

Renoprotection.
In modern nephrology, the principle of renoprotection has clearly been formed, which consists in carrying out a set of therapeutic measures in patients with kidney disease, aimed at slowing the rate of progression of CKD.

The complex of treatment measures is carried out in three stages, depending on the degree of renal dysfunction:
Stage I - nitrogen excretion function of the kidneys is preserved (CKD stages I-II), a decrease in functional reserve may be noted (no increase in GFR by 20-30% in response to a protein load).
Stage II - kidney function is moderately reduced (CKD stage III).
Stage III - kidney function is significantly reduced (CKD stage IV - beginning of stage V CKD).

Stage 1:
1. Adequate therapy for the underlying renal disease in accordance with the principles of evidence-based medicine (evaluation indicator - reduction of daily proteinuria below 2 g/day).
2. In diabetes, intensive control of glycemia and the level of glycosylated hemoglobin (evaluation indicator - control of microalbuminuria).
3. Adequate control of blood pressure and proteinuria using ACE inhibitors, ATj receptor antagonists to AII, or a combination thereof.
4. Timely and adequate treatment complications: heart failure, infections, urinary tract obstruction.
5. Exclusion of iatrogenic causes: medications, Rg-contrast studies, nephrotoxins.
6. Normalization of body weight with a mass index >27 kg/m2.
Successful pathogenetic therapy of the underlying renal disease is of paramount importance in preventing the formation of glomerulo- and tubulointerstitial sclerosis, and, consequently, in slowing the rate of progression of CKD.
In this case, we are talking not only about the treatment of newly diagnosed pathology, but also about the elimination of exacerbations.
The activity of the main inflammatory process (or its relapses) involves the activation of humoral and tissue immune reactions, naturally leading to the development of sclerosis.
In other words, the more pronounced the activity of the inflammatory process and the more often its exacerbations are noted, the faster sclerosis forms.
This statement is in full agreement with the traditional logic of the clinician and has been repeatedly confirmed by clinical studies.
In glomerular diseases, hypertension is usually formed long before the decline in renal function and contributes to their progression.
In parenchymal diseases, the tone of preglomerular arterioles is reduced and the system of their autonomous autoregulation is disrupted.
As a result, systemic hypertension leads to an increase in intraglomerular pressure and contributes to damage to the capillary bed.

When choosing antihypertensive drugs, it is necessary to proceed from the main three pathogenetic mechanisms of parenchymal renal hypertension; Na retention in the body with a tendency to hypervolemia; increased RAS activity; increased sympathetic activity nervous system due to increased afferent impulses from the affected kidney.

For any renal pathology, including diabetic nephropathy, if the creatinine level is normal and the GFR is more than 90 ml/min, it is necessary to achieve a blood pressure level of 130/85 mm Hg. Art.
If daily proteinuria exceeds 1 g/day, it is recommended to maintain blood pressure at 125/75 mm Hg. Art.
Considering modern data that nocturnal hypertension is the most unfavorable from the point of view of kidney damage, it is advisable to prescribe antihypertensive drugs taking into account these data daily monitoring blood pressure and, if necessary, reschedule their administration to the evening hours.

The main groups of antihypertensive drugs used for nephrogenic hypertension:
1. Diuretics (for GFR< 70мл/мин - преимущественно петлевые диуретики). 2. Ингибиторы АПФ и антагонисты АТ1 рецепторов к АII.
3. Non-dihydropyridine calcium channel blockers (diltiazem, verapamil).
4. Dihydropyridine CCBs are exclusively long-acting.
5. b-blockers.
Medicines are listed in descending order of recommended frequency of use.
Any antihypertensive therapy for parenchymal renal disease should begin with the normalization of Na metabolism in the body.
In kidney diseases, there is a tendency to Na retention, which is higher, the higher the proteinuria.
At least in experimental studies, the direct damaging effect of sodium contained in the diet on the glomeruli, regardless of blood pressure levels, has been proven.
In addition, sodium ions increase the sensitivity of smooth muscles to the action of AII.

The average dietary salt intake for a healthy person is approximately 15 g/day, so the first recommendation for patients with kidney disease is to limit salt intake to 3-5 g/day (an exception may be tubulointerstitial kidney damage - see above).
In an outpatient setting, a measure to monitor patient compliance with prescribed recommendations is to monitor urinary sodium excretion per day.
In cases where there is hypervolemia or the patient is not able to follow a hyposodium diet, diuretics are the first-line drugs.
If renal function is preserved (GFR > 90 ml/min), thiazides can be used; if GFR decreases< 70мл/мин назначаются петлевые диуретики (допустима комбинация петлевых диуретиков с тиазидами).
Potassium-sparing diuretics are absolutely contraindicated.

During treatment with diuretics, careful dose monitoring is necessary to prevent the development of hypovolemia. Otherwise, kidney function may acutely deteriorate - “ACF on chronic renal failure.”

Drug renoprotection.
Currently, many prospective placebo-controlled studies have proven the renoprotective effect of ACE inhibitors and AT1 receptor antagonists, which is associated with both hemodynamic and non-hemodynamic mechanisms of action of AN.

Strategy for using ACE inhibitors and/or AT1 antagonists for the purpose of nephroprotection:
- ACE inhibitors should be prescribed to all patients in the early stages of the development of any nephropathies with SPB > 0.5-1 g/day, regardless of blood pressure levels.
ACE inhibitors have renoprotective properties even at low plasma renin levels;
- the clinical predictor of the effectiveness of the renoprotective effect of drugs is partial (SPB< 2,5 г/сут) или полная (СПБ < 0,5 г/сут) ремиссия протеинурии через несколько недель или месяцев после начала приема медикаментов.
When treating with ACE inhibitors, a dose-dependence phenomenon is observed: the higher the dose, the more pronounced the antiproteinuric effect;
- ACE inhibitors and AT1 receptor antagonists have a renoprotective effect regardless of the systemic hypotensive effect.
However, if the blood pressure level does not reach the optimal level during their use, it is necessary to add antihypertensive drugs of other pharmacological groups. If you are overweight (body mass index > 27 kg/m2), it is necessary to achieve weight loss, which enhances the antiproteinuric effect of the drugs;
- if the antiproteinuric effect of any drug from one of the groups (ACE inhibitors or AT1 antagonists) is insufficient, a combination of them can be used.

The third-line drugs are non-dihydropyridine CCBs (diltiazem, verapamil). Their antiproteinuric and renoprotective effects have been proven in diabetic and non-diabetic nephropathies.
However, they can only be considered as an addition to basic therapy with ACE inhibitors or AT1 antagonists.

Less effective, from the point of view of nephroprotection, is the use of dihydropyridine CCBs.
This is associated with the ability of these drugs to dilate the glomerular afferent arterioles.
Therefore, even with a satisfactory systemic hypotensive effect, conditions are created that promote intraglomerular hypertension and, consequently, the progression of CKD.
In addition, dihydropyridine CCBs short acting activate the sympathetic nervous system, which in itself has a damaging effect on the kidney.
The negative impact of non-extended dosage forms nifedipine on the course of diabetic nephropathy.
Therefore, the use of this drug in DN is contraindicated.
On the other hand, in recent years, data have emerged indicating the effectiveness of the renoprotective properties of a combination of ACE inhibitors and long-acting dihydropyridine CCBs.

Today, b-blockers occupy the last place as renoprotective drugs.
However, in connection with recent experimental studies that have proven the role of activation of the sympathetic nervous system in the progression of chronic nephropathy, the view on the validity of their use in nephrogenic hypertension should be reconsidered.

Stage II(patient with any renal pathology and GFR 59-25 ml/min).
The treatment plan at this stage includes:
1. Dietary measures.
2. Use of loop diuretics to control hypertension and hypervolemia.
3. Antihypertensive therapy, taking into account possible side effects ACE inhibitors. If the blood plasma creatinine level is 0.45-0.5 mmol/l, do not use ACE inhibitors in high doses.
4. Correction of phosphorus-calcium metabolism disorders.
5. Early correction of anemia using erythropoietin.
6. Correction of dyslipoproteinemia.
7. Correction of metabolic acidosis. When GFR decreases below 60 ml/min (CKD stage III), all drug therapy is carried out against the background of a low-protein diet.
In order to avoid the occurrence of hypo- or hypervolemia, a more strict regimen regarding sodium and fluid intake is necessary.
Only loop diuretics are used as diuretics. Sometimes their combination with thiazides is acceptable, but the use of thiazide diuretics alone is not recommended.
It is necessary to take into account the possibility of side effects from the use of ACE inhibitors with a GFR of 59-30 ml/min, namely: deterioration of renal excretory function, which is explained by a decrease in intraglomerular pressure; hyperkalemia, anemia.
At a plasma creatinine level of 0.45-0.5 mmol/l, ACE inhibitors are not first-line drugs and are used with caution.
A combination of long-acting dihydropyridine CCBs and loop diuretics is more preferable.
When GFR is below 60 ml/min, treatment for disorders of phosphorus-calcium metabolism, anemia, dyslipoproteinemia, and acidosis begins. A low-protein diet with limited dairy products helps reduce the total amount of inorganic calcium entering the body. In addition, in CKD, the adaptive capacity of the intestine to increase calcium absorption is impaired (due to 1,25(OH)2D3 deficiency).
All these factors predispose patients to the development of hypocalcemia.
If a patient with CKD has hypocalcemia with a normal level of total blood plasma protein, it is recommended to use 1 g of pure kalysh per day exclusively in the form of calcium carbonate to correct the blood calcium level.
This type of therapy requires monitoring calcium levels in the blood and urine. Hyperphosphatemia in patients with chronic renal failure contributes to the occurrence of calcifications of soft tissues, blood vessels (aorta, aortic valve) and internal organs. It is usually recorded when GFR decreases below 30 ml/min.

A low-protein diet usually involves restricting the intake of dairy products, and therefore the intake of inorganic phosphorus into the patient’s body is reduced.
However, it should be taken into account that prolonged and significant restriction of protein intake can lead to negative protein catabolism and exhaustion.
In these cases, it is recommended to add complete proteins to the diet with the simultaneous administration of drugs that interfere with the absorption of phosphates in the intestine.

The most well-known and widely used in practice at present are calcium carbonate and calcium acetate, which form insoluble phosphate salts in the intestine.
The advantage of these drugs is the additional enrichment of the body with calcium, which is especially important for concomitant hypocalcemia. Calcium acetate is distinguished by greater phosphate-binding capacity and less release of calcium ions.

Calcium preparations (acetate and carbonate) should be taken with food, doses are selected individually and on average range from 2 to 6 g/day.
Currently, aluminum hydroxides are not used as phosphate binders due to the potential toxicity of the latter in patients with CKD.

Several years ago, phosphate binding agents that did not contain aluminum or calcium ions appeared abroad - the drug Renagel (sevelamer hydrochloride 400-500 mg).
The drug has high phosphate-binding activity; no side effects are observed with its use, but it is not registered in the Russian Federation.

In patients with CKD due to impaired endocrine renal function, there is a deficiency of the active form of vitamin D.
The substrate for the active form of vitamin D3 is 25(OH)D3 - 25-hydroxycholecalciferol, which is formed in the liver.
Kidney disease itself usually does not affect 25(OH)D3 levels, but in cases of high proteinuria, cholecalciferol levels may be reduced due to loss from vitamin D-carrying proteins.
Reasons such as insufficient insolation and protein-energy deficiency should not be ignored.
If the level of 25(OH)D3 in the blood plasma of patients with chronic renal failure is below 50 nmol/l, then patients require replacement therapy cholecalciferol.
In cases where high concentrations of parathyroid hormone (more than 200 pg/ml) are observed with normal concentrations of cholecalciferol, the use of drugs 1,25(OH)2D3 (calcitriol) or 1a(OH)D3 (alpha-calicidiol) is necessary.
The last group of drugs is metabolized in the liver to 1.25(OH)203. Low doses are usually used - 0.125-0.25 mcg based on 1,25-dihydroxycholecalciferol. This treatment regimen prevents a rise in the level of parathyroid hormone in the blood, but the extent to which it can prevent the development of hyperplasia of the parathyroid glands has not yet been clarified.

Correction of anemia
Anemia is one of the most characteristic signs of CKD.
It usually forms when GFR decreases to 30 ml/min.
The leading pathogenetic factor of anemia in this situation is an absolute or, more often, relative deficiency of erythropoietin.
However, if anemia develops in the early stages of CKD, factors such as iron deficiency (low plasma ferritin levels), blood loss in the gastrointestinal tract due to the development of erosive uremic gastroenteropathy (the most common reason), protein-energy deficiency (as a consequence of an inadequate low-protein diet or due to dietary self-restraints of the patient in the presence of severe dyspeptic disorders), lack of folic acid (a rare cause), manifestations of the underlying pathology (SLE, myeloma, etc.).

Secondary causes of anemia in CKD must be excluded whenever low hemoglobin values ​​(7-8 g/dL) are recorded in patients with GFR above 40 ml/min. In all cases, basic therapy with iron supplements (oral or intravenous) is recommended.
Currently, a common point of view has emerged among nephrologists regarding the early initiation of erythropoietin therapy for anemia.
First, experimental and some clinical studies have provided evidence that correction of anemia in CKD with erythropoietin slows the rate of progression of PN.
Secondly, early use of erythropoietin inhibits the progression of LVH, which is an independent risk factor for sudden death in chronic renal failure (especially subsequently in patients on RRT).

Treatment of anemia begins with a dose of erythropoietin 1000 units subcutaneously once a week; It is first recommended to restore iron reserves in the body (see).
The effect should be expected within 6-8 weeks from the start of treatment.
Hemoglobin levels should be maintained between 10-11 g/dL. Failure to respond to treatment usually indicates iron deficiency or intercurrent infection.
Even with a slight improvement in red blood counts, patients, as a rule, significantly improve their overall health: appetite, physical and mental performance increase.
During this period, some caution should be exercised in the management of patients, since patients independently expand their diet and are less serious about maintaining the water and electrolyte regime (overhydration, hyperkalemia).

Among the side effects of treatment with erythropoietin, a possible increase in blood pressure should be noted, which requires increased antihypertensive therapy.
Currently, when using small doses of erythropoietin subcutaneously, hypertension rarely acquires a malignant course.

Correction of dyslipoproteinemia
Uremic dyslipoproteinemia (DLP) begins to form when GFR decreases below 50 ml/min.
Its main cause is a violation of the processes of VLDL catabolism. As a result, the concentration of VLDL and intermediate-density lipoproteins in the blood increases, and the concentration of the antiatherogenic fraction of lipoproteins - high-density lipoproteins (HDL) - decreases.
In practical work, to diagnose uremic DLP, it is enough to determine the levels of cholesterol, triglycerides, and a-cholesterol in the blood. Characteristics disorders of lipid metabolism in CKD will be: normal or moderate hypercholesterolemia, hypertriglyceridemia and hypo-a-cholesterolemia.

Currently, there is an increasingly clear trend towards lipid-lowering therapy in patients with CKD.
This is explained by two reasons.
Firstly, lipid metabolism disorders in chronic renal failure are potentially atherogenic. And if we take into account that in CKD there are also other risk factors for the accelerated development of atherosclerosis (hypertension, impaired carbohydrate tolerance, LVH, endothelial dysfunction), the high mortality rate of patients with PN from cardiovascular diseases (including patients on hemodialysis) becomes understandable.
Secondly, DLP accelerates the rate of progression of renal failure in any renal pathology. Considering the nature of lipid disorders (hypertriglyceridemia, hypo-a-cholesterolemia), theoretically the drugs of choice should be fibrates (gemfibrozil).
However, their use in PN is fraught with the development of serious side effects in the form of rhabdomyolysis, since the drugs are excreted by the kidneys. Therefore, it is recommended to take small doses (no more than 20 mt/day) of 3-hydroxy-3-methylglutaryl reductase inhibitors - coenzyme A - statins, which are metabolized exclusively in the liver.
Moreover, statins also have a moderate hypotriglyceridemic effect.
The question of how lipid-lowering therapy can prevent the accelerated formation (development) of atherosclerosis in chronic renal failure remains open to this day.

Correction of metabolic acidosis
In CKD, the renal excretion of hydrogen ions, which are formed in the body as a result of the metabolism of proteins and partly phospholipids, is impaired, and the excretion of bicarbonate ions is increased.
A low-protein diet helps maintain ABS, so pronounced symptoms of metabolic acidosis occur in the later stages of CKD or in cases of non-compliance with the diet.
Typically, patients tolerate metabolic acidosis well until bicarbonate levels fall below 15-17 mmol/L.
In these cases, it is recommended to restore the bicarbonate capacity of the blood by administering sodium bicarbonate orally (1-3 g/day), and in case of severe acidosis, administering a 4% sodium bicarbonate solution intravenously.

Patients subjectively tolerate mild degrees of acidosis easily, so it is optimal to manage patients at the level of base deficiency (BE - 6-8).
With long-term oral administration of sodium bicarbonate, strict control over sodium metabolism in the body is necessary (hypertension, hypervolemia, and increased daily sodium excretion in urine are possible).
With acidosis, the mineral composition of bone tissue (bone buffer) is disrupted, and renal synthesis of 1,25(OH)2D3 is suppressed.
These factors may be important in the origin of renal osteodystrophy.

Stage III carrying out a complex of therapeutic measures in patients with CKD marks the immediate preparation of the patient for the start of renal replacement therapy.
NKF standards prescribe starting RRT when GFR is less than 15 ml/min, and in patients with diabetes it is advisable to start such treatment at more than high levels GFR, although the question of its optimal value in such a situation remains a subject of debate.

Preparing patients to start RRT includes:
1. Psychological monitoring, training, information for relatives of patients, solving employment issues.
2. Formation of vascular access (during hemodialysis treatment) - an arteriovenous fistula with a GFR of 20 ml/min, and in patients with diabetes and/or with a poorly developed venous network - with a GFR of about 25 ml/min.
3. Vaccination against hepatitis B.

Naturally, the initiation of hemodialysis or peritoneal dialysis therapy is always a drama for patients and their family members.
In this regard, psychological preparation is of great importance for subsequent treatment results.
Clarification is needed regarding the principles of the upcoming treatment, its effectiveness in comparison with treatment methods in other areas of medicine (for example, in oncology), the possibility of a kidney transplant in the future, and so on.

From the standpoint of psychological training, group therapy and patient schools are rational.
The issue of employment of patients is significant, since many patients are able and willing to continue working.
Early creation of vascular access is preferable, since the formation of an arteriovenous fistula with satisfactory blood flow requires from 3 to 6 months.

According to modern requirements, vaccination against hepatitis B should be carried out before starting hemodialysis treatment.
Vaccines against the hepatitis B virus are usually administered three times, intramuscularly, with an interval of one month after the first administration, then six months after the start of vaccination (0-1-month schedule).
A faster immune response is achieved by administering the vaccine according to the 0-1-2 month schedule. The dose of HBsAg for an adult is 10-20 mcg per injection.
Post-vaccination AT persist for 5-7 years, but their concentration gradually decreases.
When the AT titer to the surface antigen of the hepatitis B virus decreases to a level of less than 10 IU/l, revaccination is necessary.

Kidney transplant
The most promising treatment method.
Kidney transplantation is a dramatic treatment.
In perspective, the patient is healthy man, if everything goes smoothly, if the kidney is transplanted according to all the rules.
In 1952, in Boston, at the transplant center, J. Murray and E. Thomas successfully transplanted a kidney from a twin, and 2 years later - from a corpse.
This success made the surgeons Nobel Prize laureates.
The same prize was awarded to A. Carrel for his work on transplantation.
The introduction of modern immunosuppressants into transplantation practice has ensured an exponential increase in the number of kidney transplants.
Today, kidney transplantation is the most common and most successfully developing type of internal organ transplantation.
If in the 50s. While we were talking about saving patients with GN, kidneys are currently being successfully transplanted into patients with diabetic nephropathy, amyloidosis, etc.
To date, more than 500,000 kidney transplants have been performed worldwide.

Graft survival has reached unprecedented levels.
According to the United Network for Organ Allocation (UNOS) kidney registry, the 1-year and 5-year survival rates of cadaveric kidney transplants are 89.4% and 64.7%, respectively.
Similar figures for transplants from living donors are 94.5% and 78.4%.
The survival rate of patients at the same time with cadaveric transplants was 95% and 82% in 2000.
It is slightly higher in patients with kidneys transplanted from living donors - 98% and 91%.

The steady development of immunosuppression techniques has led to a significant increase in the half-life of transplants (almost 2 times).
This period is 14 and 22 years for cadaveric and living donor kidneys, respectively.
According to the Freiburg University Hospital, which summarized the results of 1086 kidney transplantations, 20 years after the operation, the survival rate of recipients was 84%, the graft functioned in 55% of those operated on.
The survival rate of grafts decreases noticeably, mainly in the first 4-6 years after surgery and especially significantly during the first year. After 6 years, the number of graft losses is negligible, so over the next 15 years the number of transplanted kidneys that maintain function remains almost unchanged.

The spread of this promising method of treating patients with end-stage CKD is hampered primarily by the shortage of donor kidneys.
A big problem in transplantation is the issue of providing donor organs.
Finding a donor is very difficult, since there are diseases that can prevent the donation of a kidney (tumors, infections, changes in the functional state of the kidneys).
It is mandatory to select a recipient based on blood type and histocompatibility antigens.
This achieves improved long-term functioning of the transplanted kidney.
This circumstance led to a significant increase in the waiting time for surgery.
Despite the high cost of immunosuppressive therapy in the postoperative period, kidney transplantation is more cost-effective than other methods of RRT.

In developed country settings, successful surgery can result in savings of approximately $100,000 over 5 years compared to a patient receiving dialysis treatment.
Despite the enormous successes of this treatment method, many issues still require further solutions.

A complex problem is the indications and contraindications for kidney transplantation.
When establishing indications for surgery, it is assumed that the course of chronic renal failure has many individual characteristics: the level of creatininemia, the rate of its increase, the effectiveness of other treatment methods, as well as complications of chronic renal failure.

A generally accepted indication for kidney transplantation is the condition of patients when the developing complications of chronic renal failure are still reversible.
Contraindications to kidney transplantation are: age over 75 years, severe pathology of the heart, blood vessels, lungs, liver, malignant neoplasms, active infection, active vasculitis or glomerulonephritis, severe degrees of obesity, primary oxalosis, uncorrectable pathology of the lower urinary tract with obstruction of urine outflow, drug or alcohol addiction, severe psychosocial problems.

Without dwelling on the purely technical details of the operation, we will say right away that the postoperative period occupies a special place in the problem of kidney transplantation, since at this time the future fate of the patient is determined.

The most important are immunosuppressive therapy, as well as the prevention and treatment of complications.
In terms of immunosuppressive therapy, the leading place belongs to “triple therapy” - GCS, cyclosporine-A (tacrolimus), mycophenolate mofetil (sirolimus).
To monitor the adequacy of immunosuppression when using cyclosporine-A and to monitor complications of treatment, the concentration of this drug in the blood should be monitored.
Starting from the 2nd month after transplantation, it is necessary to maintain the level of CSA in the blood within 100-200 μg/l.

In recent years, the antibiotic rapamycin has entered clinical practice, preventing the rejection of transplanted organs, including kidneys. Of interest is the fact that rapamycin reduces the likelihood of secondary narrowing of blood vessels after balloon angioplasty. Moreover, this medicine prevents the metastasis of certain cancers and suppresses their growth.

The results of new animal experiments at the American Mayo Clinic suggest that rapamycin increases the effectiveness of radiation treatment of malignant brain tumors.
These materials were presented by Dr. Sarkario and his colleagues in November 2002 to participants in an oncology symposium in Frankfurt.
In the early postoperative period, in addition to rejection crises, patients are threatened with infection, as well as necrosis and fistula of the bladder wall, bleeding, and the development of a steroid gastric ulcer.

In the late postoperative period, there remains a risk of infectious complications, development of graft artery stenosis, and relapse of the underlying disease in the graft (GN).
One of the pressing problems of modern transplantology is maintaining the viability of the transplanted organ.
The chances of restoring graft function are sharply reduced if the period of renal ischemia exceeds 1 hour.
Preservation of a cadaveric kidney is achieved by non-perfusion preservation in a hypothermic solution resembling intracellular fluid.